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Sida 1 från 648 resultat
Long-lasting neuropathic pain induced by brachial plexus injury in mice: Role triggered by the pro-inflammatory cytokine, tumour necrosis factor alpha.
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Brachial plexus avulsion (BPA) resulted in a marked and long-lasting mechanical hypernociception (up to 80 days) in comparison to a sham-operated group, as assessed by Von Frey filaments, in both Swiss and C57/BL6 mice. In the tail-flick test, both Swiss and C57/BL6 mice submitted to BPA showed a
The dissipation of neuropathic pain paradoxically involves the presence of tumor necrosis factor-alpha (TNF).
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Neuropathic pain, a chronic disabling pain arising from nerve injury, develops a central component. In brain neurons, tumor necrosis factor-alpha (TNF) levels intensify and TNF-inhibition of norepinephrine (NE) release, dependent upon alpha(2)-adrenergic activation, amplifies during neuropathic pain
Distinct role of tumor necrosis factor receptor subtypes 1 and 2 in the red nucleus in the development of neuropathic pain.
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Previous studies have demonstrated that tumor necrosis factor-alpha (TNF-α) in the red nucleus (RN) plays a facilitated role in the development of neuropathic pain. Here, the protein levels and roles of two different TNF receptors, p55 type 1 (TNFR1) and p75 type 2 (TNFR2), in the RN of rats with
Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice.
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Spinal cord astrocytes are critical in the maintenance of neuropathic pain. Connexin 43 (Cx43) expressed on spinal dorsal horn astrocytes modulates synaptic neurotransmission, but its role in nociceptive transduction has yet to be fully elaborated. In mice, Cx43 is mainly expressed in astrocytes,
Discovery of novel 1,2,4-triazol-5-ones as tumor necrosis factor-alpha inhibitors for the treatment of neuropathic pain.
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In this work, synthetic integration of substituted semicarbazides and various aliphatic, aryl and heteroaryl acids into 1,2,4-triazol-5-ones was accomplished. Following the assessment of neurotoxicity and peripheral analgesic activity, the compounds were evaluated in two peripheral models of
Effect of etanercept, a tumor necrosis factor-alpha inhibitor, on neuropathic pain in the rat chronic constriction injury model.
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METHODS
The effects of a low, local dose of a tumor necrosis factor-alpha (TNF-alpha) inhibitor on neuropathic pain behaviors in a rat chronic constriction injury model were evaluated.
OBJECTIVE
To investigate whether a peripherally implanted polymer drug depot can deliver a dose of etanercept
Effect of dexmedetomidine and cold stress in a rat model of neuropathic pain: Role of interleukin-6 and tumor necrosis factor-α.
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Dexmedetomidine (Dex) is a novel Alpha 2-adrenoceptor agonist. It decreases sympathetic tone and attenuates the stress responses to anesthesia and surgery. People exposed to cold suffer unpleasant thermal pain, which is experienced as stress and causes the release of noradrenaline from the
Tumor necrosis factor-alpha contributes to below-level neuropathic pain after spinal cord injury.
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OBJECTIVE
Our objective was to elucidate the mechanisms responsible for below-level pain after partial spinal cord injury (SCI).
METHODS
We used lateral hemisection to model central neuropathic pain and herpes simplex viral (HSV) vector-mediated transfer of the cleaved soluble receptor for tumor
Tumor necrosis factor receptor 1 induces interleukin-6 upregulation through NF-kappaB in a rat neuropathic pain model.
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Peripheral nerve injury resulting in neuropathic pain induces the upregulation of interleukin (IL)-6 and tumor necrosis factor-alpha, which binds to tumor necrosis factor receptor 1 (TNFR1) and induces NF-kappaB and p38 MAPK activation in the spinal cord and dorsal root ganglia (DRG). We here
[Effect of electroacupuncture on the expression of spinal glial fibrillary acidic protein, tumor necrosis factor-alpha and interleukin-1beta in chronic neuropathic pain rats].
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OBJECTIVE
To observe the effect of electroacupuncture (EA) on the expression of spinal glial fibrillary acidic protein (GFAP), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in chronic constriction injury (CCI) rats.
METHODS
Seventy-two SD rats were randomized into sham
Expression of monocyte chemoattractant protein-1 and its induction by tumor necrosis factor receptor 1 in sensory neurons in the ventral rhizotomy model of neuropathic pain.
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The expression and role of monocyte chemoattractant protein-1 (MCP-1) in the rat dorsal root ganglion (DRG) and spinal cord was evaluated in the lumbar 5 ventral rhizotomy (L5 VR) model of neuropathic pain. MCP-1 protein expression in the L4/L5 DRG neurons following L5 VR peaked after 3 days, and
Tumor necrosis factor-alpha is a potential diagnostic biomarker for chronic neuropathic pain after spinal cord injury.
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Neuropathic pain (NP) is one of the most common complications after spinal cord injury (SCI), but no protein biomarkers has ever been introduced into clinical diagnosis. Previous studies implicated that toll-like receptor (TLR) 4 played a critical role in the development of NP in animal SCI models.
Severe Radiation Necrosis Successfully Treated With Bevacizumab in an Infant with Low-Grade Glioma and Tumor-Associated Intractable Trigeminal Neuralgia.
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We present a unique case of radiation necrosis in a child with brain stem low-grade glioma (LGG) presenting with trigeminal neuralgia. Despite extensive therapies, severe pain persisted. She received proton beam radiation with significant improvement. However, she developed radiation necrosis and
Possible association of lower rate of postherpetic neuralgia in patients on anti-tumor necrosis factor-α.
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Recently, a study of patients with rheumatoid arthritis who developed herpes zoster while taking a tumor necrosis factor (TNF)-α inhibitor reported a decreased incidence of postherpetic neuralgia. The objective of this study was to investigate whether patients on TNF-α inhibitors who developed
Intraneural injection of interleukin-1beta and tumor necrosis factor-alpha into rat sciatic nerve at physiological doses induces signs of neuropathic pain.
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Proinflammatory cytokines are mediators of inflammatory and neuropathic pain. Here, we investigated pain-related behavior in rats after intraneural injection of different doses of rat recombinant interleukin-1beta (rrIL-1beta) and tumor necrosis factor-alpha (rrTNF) into the sciatic nerve. Doses
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